our shown that SVT induced apoptosis is in conjunction with DR4 and DR5. The a cancerous colon cells were treated with snake venom toxin for 24 h, and then labeled with TUNEL solution. Total number of cells in a given region was determined by applying MAPK phosphorylation DAPI nuclear staining. The apoptotic index was determined because the DAPI stained TUNEL good cell number/total DAPI stained cell number. Tips, method of three studies, with triplicates of each test, bars, SD., p 0. 05, significantly different from snake venom toxin untreated control cells. 5 of 12 suggesting that ROS is also involved with snake venom toxininduced upregulation and apoptosis of DRs, and activation of JNK. Taken together, these indicated that the JNK and ROS process are essential in induction of DR4 and DR5 expression, and DR4 and DR5 mediated apoptosis by snake venom toxin in cancer of the colon cells. We confirmed that snake venom toxin inhibited HCT116 and HT 29 colon cancer cell growth through apoptosis. Our study also showed this effect was associated with the JNK and ROS mediated enhanced expression of the DR5 and DR4. The Papillary thyroid cancer TRAIL receptors, DR4 and DR5 are also expressed in colon carcinomas and their expressions are improved as tumor cells acquire malignant potential. Tumor and cancer of the colon cells are relatively painful and sensitive to TRAIL mediated apoptosis, but standard colonic epithelium are immune to TRAILmediated apoptosis. Due to its particular capacity for killing of cyst cells with small negative effects on normal cells, the activators of TRAIL pathway have emerged as desirable candidates for cancer therapy. It has been proven that TRAIL induced apoptosis could be enhanced by chemotherapy in many in vitro and xenograft Dub inhibitor types of cancer, an effect claimed to be mediated through enhanced DR4 and DR5 term. . Like, Garcinol produced from dried rind of the good fresh fruit Garcinia indica includes a synergistic anticancer impact with TRAIL by up regulate the DR4 and DR5 in human colon cancer cells. Celastrol, a triterpenoid isolated from the standard Chinese medicine promotes TRAIL induced apoptosis through the upregulation of DRs in cancer of the colon cells. Diosgenin, a steroid saponin within fenugreek induced apoptosis in colon cancer cells and sensitized colon cancer cells to TRAIL by induction of DR5. Recent reports indicate that DR levels may be improved by endogenous induction or exogenous overexpression. A few genotoxic and nongenotoxic agents may induce apoptosis by increasing endogenous DRs. On another hand, exogenously overexpressed DRs, without concomitant up-regulation in its ligand levels, have now been shown to be related to induction of apoptosis. Similar to previous reports, we showed that the snake venom toxin caused DR4 and DR5 in colon cancer cells, however the expression of Fas and other death Figure 2 Effect of snake venom toxin on ROS generation and the expression of death receptors in human colon cancer cells.